[Contribution to the study of the humoral manifestations of pain. Effect of pain on the sanguine acid-base equilibrium and blood ascorbic acid].
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Acid-Base Equilibrium↗
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[Contribution to the study of the humoral manifestations of pain. Effect of pain on the sanguine acid-base equilibrium and blood ascorbic acid content of the blood].
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Acid-Base Equilibrium↗
Short-term ascorbic acid deficiency induced oxidative stress in the retinas of young Guinea pigs.
We examined whether short-term ascorbic acid deficiency induces oxidative stress in the retinas of young guinea pigs. Four-week-old guinea pigs were given a scorbutic diet (20 g/animal/day) with and without adequate ascorbic acid (400 mg/animal/day) in drinking water for 3 weeks. The serum concentrations of the reduced form of ascorbic acid and the oxidized form of ascorbic acid in the deficient group were 14.1 and 4.1%, respectively, of those in the adequate group. The retinal contents of the reduced form of ascorbic acid and the oxidized form of ascorbic acid in the deficient group were 6.4 and 27.3%, respectively, of those in the adequate group. The retinal content of thiobarbituric acid-reactive substances, an index of lipid peroxidation, was 1.9-fold higher in the deficient group than in the adequate group. Retinal reduced glutathione and vitamin E contents in the deficient group were 70.1 and 69.4%, respectively, of those in the adequate group. This ascorbic acid deficiency did not affect serum thiobarbituric acid-reactive substances and reduced glutathione concentrations but increased serum vitamin E concentration. These results indicate that short-term ascorbic acid deficiency induces oxidative stress in the retinas of young guinea pigs without disrupting systemic antioxidant status.
Animals↗
Protective effect of lipophilic derivatives of ascorbic acid on lipid peroxide-induced endothelial injury.
The protective effects of ascorbic acid and its lipophilic derivatives on the cytotoxicity of linoleic acid hydroperoxide (LOOH), a primary product of lipid peroxidation, was investigated in cultured human umbilical vein endothelial cells. When cells were incubated with ascorbic acid for 24 h before treatment with LOOH, ascorbic acid did not protect cells from oxidative damage by LOOH. Its lipophilic derivatives such as 6-O-palmitoyl,6-O-stearoyl, and 2,6-O-dipalmitoyl esters and 2-O-octadecyl ether (CV3611) had an apparent protective effect on the toxicity of LOOH. When cells were incubated in medium containing both antioxidant and LOOH, the protective effect of lipophilic derivatives became weak. An interaction between alpha-tocopherol and ascorbic acid was not observed in this system using endothelial cells. However, in the case where the cells were preincubated with alpha-tocopherol and 6-O-palmitoylascorbic acid, the ascorbic acid derivative had a synergistic effect to alpha-tocopherol in protecting against LOOH-induced damage. These results suggest that lipophilic antioxidants incorporated into cellular membranes are effective protectors against LOOH, whereas lipophobic antioxidants located outside the membrane do not have any protective effect.
Ascorbic Acid↗
Renal excretion of ascorbic acid: effect of age and sex.
To determine if the lower plasma ascorbic acid concentrations observed in males compared to females, and in the elderly in general, might be due to differences in renal clearances of ascorbic acid, tubular maximum reabsorptions (TmAA) and renal thresholds for ascorbic acid were determined on older (10 male, 10 female, aged 70-86 years) and younger (3 male, 5 female, aged 26-59 years) subjects. The mean TmAA for men was 1.54 +/- 0.29 and for women 1.39 +/- 0.33 mg/minute/100 mL glomerular filtration rate (p > 0.05). The mean renal threshold for men was 1.51 +/- 0.25 and for women 1.26 +/- 0.16 mg/dL (p < 0.02). Neither was affected by age. If differences in TmAA and renal threshold were to explain the lower plasma ascorbic acid concentrations observed in males, both values should have been lower than in females. The ability of women to maintain higher plasma ascorbic acid concentrations than men, and young higher than elderly, cannot be explained by differences in the renal handling of ascorbic acid.
Adult↗
Status of ascorbic acid in iron deficiency anaemia and thalassaemia.
The status of ascorbic acid was studied at the levels of platelet and leucocyte in 32 cases of iron deficiency anaemia, 35 cases of thalassaemia and 18 normal subjects. It was found that in iron deficiency anaemia, platelet ascorbic acid was significantly higher than normal values indicating tissue excess and came down sharply after treatment with iron. In thalassaemia, associated presumably with iron overload, ascorbic acid status of platelets was definitely lower than normal indicating tissue deficiency. Leucocytic level of ascorbic acid was not as good an index of ascorbic acid status as the platelet level.
Anemia, Hypochromic↗
Effect of ascorbic acid supplementation on selenium bioavailability in humans.
The study was designed to investigate the effect of supplemental ascorbic acid on the bioavailability of selenium (Se) in humans by using plasma Se levels and plasma glutathione peroxidase (GSH-Px) activity as indicators of the body Se status. Three groups of female university students were supplemented for 4 weeks with either 50 micrograms sodium selenate, 50 micrograms sodium selenate together with 200 mg ascorbic acid, or with 200 mg ascorbic acid three times daily during meals. Plasma Se levels increased significantly (P less than 0.01) in all three groups regardless of the type of supplementation. The increase was highest in the group having both Se and ascorbic acid and smallest in the group receiving only ascorbic acid. The changes in plasma GSH-Px activities reflected those in plasma Se, but the increases were smaller (P less than 0.05). These results suggest that supplemental ascorbic acid may have a beneficial effect on the bioavailability of the natural Se in foods. However, ascorbic acid did not seem to affect the availability of the supplemental sodium selenate. Therefore, the effect of ascorbic acid on the bioavailability of selenium may vary depending on the ingested selenium compound.
Adult↗
Oxidation in fish oil enriched mayonnaise: ascorbic acid and low pH increase oxidative deterioration.
The effect of ascorbic acid (0-4000 ppm) and pH (3.8-6.2) on oxidation and levels of iron and copper in various fractions of mayonnaise enriched with 16% fish oil was investigated. Ascorbic acid induced release of iron from the assumed oil-water interface into the aqueous phase at all pH levels, but this effect of ascorbic acid was strongest at low pH (pH 3.8-4.2). Ascorbic acid generally promoted formation of volatile oxidation compounds and reduced the peroxide value in mayonnaises. Peroxide values and total volatiles generally increased with decreasing pH values, suggesting that low pH promoted oxidation. It is proposed that iron bridges between the egg yolk proteins low-density lipoproteins, lipovitellin, and phosvitin at the oil-water interface are broken at low pH values, whereby iron ions become accessible as oxidation initiators. In the presence of ascorbic acid, oxidation is further enhanced due to the reduction of Fe(3+) to Fe(2+) that rapidly catalyzes lipid oxidation via lipid hydroperoxide decomposition at the oil-water interface in mayonnaise.
Antioxidants↗
Decreased expression of the vitamin C transporter SVCT1 by ascorbic acid in a human intestinal epithelial cell line.
Vitamin C (ascorbic acid) is an essential nutrient that is involved in a number of cellular processes. However, unlike most mammals, man is unable to synthesize vitamin C and it must therefore be acquired from the diet. Absorption of vitamin C is achieved by two transporters, SVCTI and SVCT2, recently cloned from rat and human kidney. SVCT1 is thought to be the predominant transporter in the intestine. Vitamin C supplements are increasingly common, thus contributing to an increased dietary load, and therefore the aim of the present study was to investigate the effect of high doses of ascorbic acid on SVCT1 expression. Using the Caco-2 TC7 cell model of small intestinal enterocytes, we measured the effects of ascorbic acid (4.5 mg/ml culture medium) on L-[14C]ascorbic acid uptake and SVCT1 expression (determined by reverse transcription-polymerase chain reaction). Ascorbic acid uptake was decreased significantly in Caco-2 TC7 cells exposed to ascorbate for 24 h (-50%, P<0.0005). Expression of SVCT1 was also significantly reduced by exposure to elevated levels of ascorbate for 24h (-77%, P<0.005). Taken together these results suggest that high-dose supplements might not be the most efficient way of increasing the body pool of vitamin C.
Ascorbic Acid↗
Effects of ascorbic acid on the antifungal action of amphotericin B.
Ascorbic acid enhanced the lethal but not the permeabilizing effects of amphotericin B on Candida albicans and Cryptococcus neoformans cells. Two other ene-diol acids, D-erythorbate and dihydroxyfumarate, also enhanced the lethal action of amphotericin B on Can. albicans. Maleic acid and gulanolactone, compounds structurally related to ascorbic acid but not containing the ene-diol group, had no such effect. It is assumed that ascorbic acid and the two other ene-diol acids acting as pro-oxidants augmented the oxidation-dependent killing of fungal cells induced by amphotericin B.
Amphotericin B↗
Decrease in bone density in young male guinea pigs fed high levels of ascorbic acid.
These experiments were conducted to investigate the effects of high oral intakes of ascorbic acid on bone metabolism in young guinea pigs and to inquire into the mechanism mediating these effects. Male guinea pigs 14 days old fed 8.7% of ascorbic acid for 6 weeks had decreased bone density and decreased urinary hydroxyproline compared to control animals fed 0.2% of ascorbic acid. To assess whether these changes were due to the acidity of the diet or to vitamin activity, salts of ascorbic acid, salts of erythorbic acid and free erythorbic acid were fed. There were no significant bone changes in any of these groups. The results strongly indicate that the acidity of ascorbic acid plays a part in the decrease in bone density but do not rule out that some other metabolic property specific to ascorbic acid may also be implicated.
Aging↗
Ascorbic acid in the prevention and treatment of cancer.
Proposed mechanisms of action for ascorbic acid (ascorbate, vitamin C) in the prevention and treatment of cancer include enhancement of the immune system, stimulation of collagen formation necessary for "walling off" tumors, inhibition of hyaluronidase which keeps the ground substance around the tumor intact and prevents metastasis, prevention of oncogenic viruses, correction of an ascorbate deficiency often seen in cancer patients, expedition of wound healing after cancer surgery, enhancement of the effect of certain chemotherapy drugs, reduction of the toxicity of other chemotherapeutic agents such as Adriamycin, prevention of free radical damage, and neutralization of carcinogenic substances. Scottish as well as Japanese studies have pointed to the potential benefit of high dose vitamin C for the treatment of "terminal" cancer. Mayo Clinic studies, however, have contradicted the Scottish and Japanese findings, resulting in accusations of methodological flaws from both sides. Numerous epidemiological studies have pointed to the importance of dietary and supplemental ascorbate in the prevention of various types of cancer including bladder, breast, cervical, colorectal, esophageal, lung, pancreatic, prostate, salivary gland, stomach, leukemia, and non-Hodgkin's lymphoma.
Ascorbic Acid↗
Morphological and biochemical alterations of oomycete fish pathogen Saprolegnia parasitica as affected by salinity, ascorbic acid and their synergistic action.
Vegetative growth of Saprolegnia parasitica decreased by increasing the concentration of NaCl and ascorbic acid. Under these conditions, the morphological features of the vegetative hyphae were distinguishable from those used as controls. NaCl and ascorbic acid in combination improved the tolerance of S. parasitica to high levels of salinity. Sporangial formation, release and proliferation were very sensitive to even lower levels of salinity. For instance, at 0.03 M NaCl sporangia formation was rarely observed. Ascorbic acid alone had a little effect on sporangial formation and release, but when combine with NaCl the developmental processes were improved. Reduction of numbers and plasmolysis of oogonia were found at various NaCl concentrations, whereas ascorbic acid stimulated the formation of these reproductive organs at low concentrations. The synergistic effect of NaCl and ascorbic acid improved and overcomed the symptoms of oogonial plasmolysis. Protease activity of S. parasitica was significantly reduced at all NaCl concentrations, whilst ascorbic acid significantly increased and inhibited it at low concentrations and at moderate and high concentrations, respectively. The combination of these compounds reduced protease activity at all tested concentrations with significant difference at the highest concentration. The total free amino-acids content of S. parasitica mycelia was significantly reduced at all the NaCl concentrations, whereas ascorbic acid significantly increased it at low but inhibited it at higher concentrations. The combination of NaCl and ascorbic acid significantly increased the accumulation of free amino-acids at low and moderate concentrations, but decreased them at high concentrations. Total protein content was reduced at all tested concentrations of NaCl and ascorbic acid had also similar effect. However, the combined effect of NaCl and ascorbic acid significantly enhanced and reduced total protein content at low and high concentrations, respectively. Treatments with NaCl induced proline accumulation in S. parasitica, which paralleled the salt concentration.
Animals↗
Ascorbic acid intakes and plasma levels in healthy elderly.
The data presented show that elderly men have significantly lower plasma ascorbic acid concentrations than elderly women at similar intakes of ascorbic acid. We hypothesize that this difference is due to lower renal tubular reabsorption of ascorbic acid in elderly men. The finding that more than half of the healthy elderly men had plasma ascorbic acid levels less than 0.3 mg/dl with daily intakes of ascorbic acid in the range of 40 to 50 mg raises concern about the rationale of lowering the RDA for vitamin C from the current value of 60 mg to 40 mg for men and 30 mg for women. This recommendation is inconsistent with efforts to improve the health status of elderly Americans by assuring adequate intakes of all essential nutrients. Our data do not allow us to determine an optimal intake of ascorbic acid for the elderly. The possibility of increased health benefits associated with intakes that exceed the current RDA of 60 mg needs to be examined. We believe, however, that a prudent approach to both of these questions would be to recommend that elderly receive a daily ascorbic acid intake that would allow plasma concentration to be maintained at or near 1.0 mg/dl. The daily level of intake required to maintain this level would be approximately 125 mg and 75 mg in healthy elderly men and women respectively. These intakes would assure adequate body reserves of ascorbic acid.
Aged↗
Ascorbic acid synthesis in fetal and neonatal pigs and in pregnant and postpartum sows.
The ontogeny of ascorbic acid synthesis and its concentration in fetal pigs from mid- to late gestation, and the effect of birth order and premature or normal delivery ages were evaluated. In Experiment 1, fetal pigs were collected from three sows at 60, 80, 100, 107 and 111 d of development. Liver L-gulono-gamma-lactone oxidase (GLO) activity and ascorbic acid concentration were measured. High liver GLO activity in fetal liver occurred at 60 d but declined as pregnancy advanced (P < 0.01), whereas ascorbic acid concentration increased (P < 0.01). Experiment 2 evaluated ascorbic acid synthesis and concentration in neonates born early (1st and 2nd) or late (7th and 8th) in the birthing sequence, or when born 2 d prematurely vs. the normal delivery age. Pigs born early in the birthing sequence (P < 0.01) and those born at the natural delivery age (P < 0.05) had higher liver ascorbic acid concentrations, but liver GLO activity did not differ among groups. Sows were killed at each period; liver GLO activity was constant during gestation but increased postpartum (P < 0.01). Liver ascorbic acid concentration was constant during gestation, except for a decline during late gestation, and increased postpartum (P < 0.05). These results suggest that more ascorbic acid was transferred from the dam to the fetuses as pregnancy advanced, possibly suppressing fetal GLO activity. Thus, fetal liver GLO activity was the primary source of ascorbic acid during early fetal development, but more fetal ascorbic acid was transferred from the dam during later pregnancy.
Animals↗
The effects of ascorbic acid deficiency on calcium and collagen metabolism in cultured fetal rat bones.
The effects of ascorbic acid deficiency on growth and calcification of bone were studied in whole 18-day fetal rat radii and ulnae cultured in a chemically defined medium. Ascorbic acid deficiency decreased the formation of labeled hydroxyporline from labeled proline in both bone shafts and cartilage ends while incorporation of tryptophan was maintained. Dry weights and collagen content of bone and cartilage were decreased, but calcification was not affected. The optimun initial concentration of ascorbic acid for collagen synthesis was 200 mug/ml. The effect of ascorbic acid was not antagonized by glucoascorbic acid or replaced by dithiothreitol. Decreased collagen synthesis in ascorbic acid deficiency could not be ascribed to loss of available peptidyl proline hydorxylase. Formation of underhydroxylated collagen and its release into the medium accounted for much of the decrease in hydroxylated collagen in ascorbic acid deficient bones. Nevertheless, the total newly synthesized collagen, as measured by collagenase digestion, was still decreased. Similar effects were exerted by alpha, alpha'-dipyridyl which also inhibited general protein synthesis. Ascorbic acid did not stimulate proline incorporation into collagen in the presence of alpha, alpha'-dipyridyl.
Animals↗
Ascorbic acid increases the severity of spontaneous knee osteoarthritis in a guinea pig model.
OBJECTIVE: To determine whether ascorbic acid might be of benefit for the treatment of spontaneous osteoarthritis (OA) when administered over a long period of time. METHODS: We investigated the effects of 8 months' exposure to low, medium, and high doses of ascorbic acid on the in vivo development of histologic knee OA in the male Hartley guinea pig. The low dose represented the minimum amount needed to prevent scurvy. The medium dose was the amount present in standard laboratory guinea pig chow and resulted in plasma levels comparable with those achieved in a person consuming 200 mg/day (5 fruits and vegetables daily). The high dose was the amount shown in a previous study of the guinea pig to slow the progression of surgically induced OA. RESULTS: We found an association between ascorbic acid supplementation and increased cartilage collagen content but, in contrast to findings in a previous study of surgically induced OA in the guinea pig, ascorbic acid worsened the severity of spontaneous OA. Active transforming growth factor beta (TGF beta) was expressed in marginal osteophytes, whose size and number were significantly increased with increasing intake of ascorbic acid. Synovial fluid levels of cartilage oligomeric matrix protein, a biomarker of cartilage turnover, corroborated the histologic findings. CONCLUSION: Ascorbic acid has been shown to activate latent TGF beta. Prolonged intraarticular exposure to TGF beta has been shown to cause OA-like changes. We found expression of active TGF beta in osteophytes, a prominent feature of the joint histology seen in association with ascorbic acid treatment. Thus, the deleterious effects of prolonged ascorbic acid exposure may be mediated in part by TGF beta. This worsening of OA with ascorbic acid supplementation suggests that ascorbic acid intake should not be supplemented above the currently recommended dietary allowance (90 mg/day for men and 75 mg/day for women).
Animals↗
Regulation of growth, protein synthesis, and maturation of fetal bovine epiphyseal chondrocytes grown in high-density culture in the presence of ascorbic acid, retinoic acid, and dihydrocytochalasin B.
Phenotypic expression of chondrocytes can be modulated in vitro by changing the culture technique and by agents such vitamins and growth factors. We studied the effects of ascorbic acid, retinoic acid (0.5 and 10 microM), and dihydrocytochalasin B (3, 10, 20 microM DHCB), separately or in combination (ascorbic acid + retinoic acid or ascorbic acid + DHCB), on the induction of maturation of fetal bovine epiphyseal chondrocytes grown for up to 4 weeks at high density in medium containing 10% fetal calf serum and the various agents. In the absence of any agent or with retinoic acid or DHCB alone, the metabolic activity of the cells remained very low after day 6, with no induction of type I or X collagen synthesis nor increase in alkaline phosphatase activity. Chondrocytes treated with fresh ascorbic acid showed active protein synthesis associated with expression of types I and X after 6 and 13 days, respectively. This maturation was not accompanied by obvious hypertrophy of the cells or high alkaline phosphatase activity. Addition of retinoic acid to the ascorbic acid-treated cultures decreased the level of type II collagen synthesis and delayed the induction of types I and X collagen, which were present only after 30 days. A striking increase in alkaline phosphatase activity (15-20-fold) was observed in the presence of both ascorbic acid and the highest dose of retinoic acid (10 microM). DHCB was also a potent inhibitor of the maturation induced by treatment with ascorbic acid, as the chondrocytes maintained their rounded shape and synthesized type II collagen without induction of type I or X collagen. The pattern of protein secretion was compared under all culture conditions by two-dimensional gel electrophoresis. The different regulations of chondrocyte differentiation by ascorbic acid, retinoic acid, and DHCB were confirmed by the important qualitative and quantitative changes in the pattern of secreted proteins observed by two-dimensional gel electrophoresis along the study.
Animals↗